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Death rates were, however, available only in 5-year age ranges, within which fluctuations in mean age can cause appreciable artifactual fluctuations in mortality. For —, the artifactual mortality fluctuations in particular 5-year age ranges for a reasonably stable cause of death eg, female non-respiratory cancer can be used to help quantify the expected artifactual effects for overall mortality.

This suggests that such artifacts were negligible at ages 15—34 years and 55—74 years, and suggests that even at ages 35—54 years where they slightly accentuated the decreases in —88 and —98 and the increases in —94 and —99 in overall mortality , any such artifacts were an order of magnitude smaller than the real changes in overall mortality.

Evidence of a major effect of alcohol consumption on recent Russian mortality patterns comes from both cause-specific analyses of national mortality trends 4—10 and analytical studies of individuals. Overall mortality rates and the distribution of the main certified causes of death were similar to those in the whole of Russia, and fluctuated in a similar way during the s, with a sudden large increase in mortality during — Such records include virtually all urban deaths but, until , excluded deaths of migrants to the three cities.

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For each death record we ignored the local death coding, 5 and used the International Classification of Diseases and Related Health Problems 10th revision ICD to assign the underlying cause from the written death certificate. During —05, teams of local physicians were trained in objective interview methods and worked under supervision mainly in those areas of town in which at least one had practised although most were currently not doing so; this study was not identified with local health-care services. Questions about decedents did not dominate the interview, since interviewers first completed standard questionnaires about smoking, drinking, and other factors for all adults present for future prospective study.

A fixed sequence was used to select a competent adult informant for the deceased individual; spouses were the first choice, then siblings, then parents, then adult children, then any other adult family member. Informants could be blood or in-law relatives living at the address. One in ten interviews about decedents was randomly chosen for repetition to monitor performance. Alcohol questions did not obtrude, because much other information was obtained, including ethnicity, marital status, education level, jobs held, job loss, income, recent changes in income, and smoking usual daily amount, age started, age stopped.

Smokers were defined as those who had smoked within 5 years of death or after age 55 years. The questionnaire used in the interview asked about usual alcohol consumption patterns before the final year of life usual weekly frequency of drinking spirits, beer, and wine, usual amounts of each per session, and maximum amount [just of spirits] per session. Total weekly alcohol consumption frequencies multiplied by usual amounts was expressed in mL bottles of vodka or alcoholic equivalent. The same questions were asked about the final year of life, but the usual amounts reported for the two periods were similar, and only the greater of the two was used.

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Alcohol intake is difficult to assess reliably in proxy interviews several years after death. Moreover, if death was from a disease or external cause substantially affected by alcohol, families might tend to misreport amounts or even report no alcohol use, leading some drinkers to be misclassified as never-drinkers. Since real never-drinking is rare in Russia, at least in men, this could make the ratio of proxy-reported never-drinkers to ever-drinkers differ substantially between those who died from alcohol-affected diseases or external causes and other diseases.

The main case—control analyses therefore ignore the small numbers reported as never-drinkers, compare the four categories of ever-drinkers, and make approximate correction for the effects of uncertainty in alcohol use. Sensitivity analyses include the never-drinkers. The case—control comparisons relate alcohol consumption category reference or other among ever-drinkers to underlying cause of death case or control. Cases were those who had died from the causes that, in our prior judgment, could be substantially affected by alcohol or tobacco: alcohol poisoning redefined to include the few deaths from alcoholic psychosis , other external causes, ill-defined causes, tuberculosis, respiratory disease, vascular disease, oesophagus, stomach, liver, or pancreas disease apart from diabetes mellitus and lung, upper aerodigestive tract, stomach, liver, pancreas, bladder, or breast cancer.

Controls were those adults who had died from other diseases, including some malignant neoplasms, all benign neoplasms, diabetes, diseases of the nervous system, non-alcoholic mental disorders, renal disease, and all infectious or parasitic diseases other than tuberculosis, pneumonia, or hepatitis. The main analyses are of ever-drinkers, and compare four alcohol categories. Sensitivity analyses involved cruder alcohol categories but more stratification.

The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report. The corresponding authors had full access to all the data in the study and had final responsibility for the decision to submit for publication.

Within each category, however, male and female controls had similar consumption patterns. Table 2 gives the main results for male mortality at ages 15—74 years in ever-drinkers, subdivided by cause and amount drunk. Male relative risk of death at ages 15—74 years, by proxy-reported alcohol intake other drinkers vs reference drinkers, excluding never-drinkers and certified cause other causes vs control diseases.

The latter two groups include some misclassified deaths that were actually from alcohol poisoning.

Table 3 gives the corresponding results for women. For neoplastic disease, the RR in the highest drinking category appeared to be increased only for liver cancer and upper aerodigestive tract cancer, although no trend in cancer mortality was significantly positive perhaps because of small numbers. Female relative risk of death at ages 15—74 years, by proxy-reported alcohol intake other drinkers vs reference drinkers, excluding never-drinkers and certified cause other causes vs control diseases. The same findings were seen for each main group of external causes, including transport accidents, other accidents, suicide, and assault.

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Again, the RR was substantially less extreme for acute myocardial infarction than for other acute IHD, and in the top two alcohol consumption categories, only 64 women died from acute myocardial infarction compared with from other acute IHD. Table 4 subdivides the results for all men more narrowly by age 15—54 years and 55—74 years and groups the causes as alcohol poisoning, accidents and violence, diseases strongly associated with alcohol in this study, other non-control diseases, and control diseases.

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The relative risks comparing never-drinkers with reference drinkers are consistent with families under-reporting moderate alcohol use more in men who had died from accidents, violence, and diseases strongly associated with alcohol than in men who had died from other diseases. Male dose-related excess mortality in ever-drinkers as a proportion of all mortality in male ever-drinkers and never-drinkers, by age and underlying cause of death.

Table 5 gives corresponding results for women. Discrepancies between never-drinkers and reference drinkers are less extreme than in men, but are still apparent, particularly at ages 55—74 years. Female dose-related excess mortality in ever-drinkers as a proportion of all mortality in female ever-drinkers and never-drinkers, by age and underlying cause of death. The relative risks in ever-drinkers which compare the three higher alcohol consumption categories with the reference category might be more directly indicative of real associations.

Even in ever-drinkers, however, substantial misclassification of real alcohol consumption patterns is inevitable. If some alcohol-associated deaths are included in the reference category, then uncorrected calculation of alcohol-dose-related excess mortality in the other three alcohol consumption categories will underestimate the real excess mortality. These corrected percentages are similar to those shown in tables 4 and 5 , and were not materially affected by finer stratification for potential confounders amount smoked, year of death, years since death, marital status, relationship to informant, ethnicity, education, occupation, socioeconomic status, or recent change in socioeconomic status or by inclusion in the controls of all cancers not strongly related to alcohol data not shown.

Non-beverage alcohol use was strongly correlated with other alcohol use but, given vodka consumption, was no more common in those dying from strongly alcohol-related causes than in those dying from other causes. These findings suggest that for a given amount of ethanol consumption its source was not strongly predictive of cause of death. Figure 2 shows the regional mortality trends — in mortality from all causes, from the main causes strongly associated with alcohol use in this study approximately as in table 2 , and from the other causes.

Because of the changes in Russian death coding in , the strongly alcohol-related causes had to include chronic heart disease and exclude liver cancer see panel 2. In both sexes and all age-groups there was a much sharper increase during —94 in mortality from the strongly alcohol-related causes than from other causes. Fluctuations in these alcohol-related causes were the main determinants of the large fluctuations in all-cause mortality in the study areas, particularly at ages 15—34 years and 35—54 years.

Thus, at these ages, the ratio of mortality from the strongly alcohol-related causes to mortality from all other causes fluctuated sharply, and was at a maximum in This was true for the whole study region figure 2 and for the individuals in our study data not shown. Mortality from all causes, from causes strongly related to alcohol, and from other causes in the Altay and Tomsk regions of Russia, — See panel 2 for definition of causes.

The death rate R per in each year age range is the mean of the annual rates in the four 5-year age ranges. Source: regional mortality and population estimates.


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The strongly alcohol-related causes included in our analyses of regional time trends differ slightly from those used in all of our other analyses, because they had to be defined from Russian cause of death codes, 6 which changed in but still differed from the International Classification of Diseases, 10th revision. We found strong dose-response associations between alcohol consumption and mortality from accidents, violence, and several disease groupings.

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  • If these associations are mainly causal, then alcohol was responsible for more than half of all deaths in younger men 15—54 years in our study areas during —, and was a major cause of death in older men 55—74 years and in women. Additionally, large fluctuations in mortality from alcohol-related diseases were major determinants of the extreme fluctuations in overall adult mortality after , so the proportion of deaths caused by alcohol would be much greater in some years than in others.

    Our study of residents in three industrial cities populated mainly by European Russians was large and population based. The interviewers were local physicians; therefore, few families refused to be interviewed and cooperation was generally good. Information was unavailable only when the address no longer existed or no family member was found there.

    This excludes deaths in families that subsequently moved, deaths of those who perhaps partly because of alcohol were isolated or without a registered address, and deaths of migrants to the study cities. Otherwise, selection bias is unlikely to have had any major affect on the results. Cases were those adults who had died from causes we judged beforehand likely to be related to drinking or smoking, and controls were those who had died from other causes.

    This designation of controls was somewhat arbitrary, but is supported by the cancer results. The extensive epidemiological evidence on alcohol and cancer, as summarised by the WHO International Agency for Research on Cancer IARC , 19 shows that the only major types of cancer much affected by alcohol in men are those of the liver and upper aerodigestive tract.

    This evidence helps validate the case—control results from our study table 2 , which show a highly significant effect of alcohol on mortality from cancers of the liver and upper aerodigestive tract, but not from lung cancer or stomach cancer. Few women consumed more than three bottles of vodka or equivalent per week, but among those who did, the only conventionally significant excess cancer risks were for those of the liver and upper aerodigestive tract.

    Use of deceased people as controls was intended to limit the effects of recall and reporting bias, with the expectation that there would be no large systematic bias between people with similar drinking habits who had died of different diseases. Similarly, many epidemiological studies of hospitalised cases use hospitalised controls. Although families in our study are likely to misreport alcohol consumption, we had hoped that such misreporting would merely dilute the strengths of any associations. We found, however, that under-reporting of moderate alcohol consumption was particularly common for those who had died from accidents, violence, and the diseases strongly related to drinking.

    This under-reporting could substantially distort relative risks comparing never-drinkers with reference drinkers, but should have less of an effect on the corrected dose-related excess, on which our main conclusions are based.